Sian M J Hemmings, Patricia Swart, Jacqueline S Womersely, Ellen S Ovenden, Leigh L van den Heuvel, Nathaniel W McGregor, Stuart Meier, Soraya Bardien, Shameemah Abrahams, Gerard Tromp, Robin Emsley, Jonathan Carr, Soraya Seedat
{"title":"创伤后应激障碍、帕金森病和精神分裂症基因表达谱的RNA-seq分析确定了常见和独特的生物学途径的作用","authors":"Sian M J Hemmings, Patricia Swart, Jacqueline S Womersely, Ellen S Ovenden, Leigh L van den Heuvel, Nathaniel W McGregor, Stuart Meier, Soraya Bardien, Shameemah Abrahams, Gerard Tromp, Robin Emsley, Jonathan Carr, Soraya Seedat","doi":"10.1007/s44192-022-00009-y","DOIUrl":null,"url":null,"abstract":"<p><p>Evidence suggests that shared pathophysiological mechanisms in neuropsychiatric disorders (NPDs) may contribute to risk and resilience. We used single-gene and network-level transcriptomic approaches to investigate shared and disorder-specific processes underlying posttraumatic stress disorder (PTSD), Parkinson's disease (PD) and schizophrenia in a South African sample. RNA-seq was performed on blood obtained from cases and controls from each cohort. Gene expression and weighted gene correlation network analyses (WGCNA) were performed using DESeq2 and CEMiTool, respectively. Significant differences in gene expression were limited to the PTSD cohort. However, WGCNA implicated, amongst others, ribosomal expression, inflammation and ubiquitination as key players in the NPDs under investigation. Differential expression in ribosomal-related pathways was observed in the PTSD and PD cohorts, and focal adhesion and extracellular matrix pathways were implicated in PD and schizophrenia. We propose that, despite different phenotypic presentations, core transdiagnostic mechanisms may play important roles in the molecular aetiology of NPDs.</p>","PeriodicalId":72827,"journal":{"name":"Discover mental health","volume":" ","pages":"6"},"PeriodicalIF":0.0000,"publicationDate":"2022-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10501040/pdf/","citationCount":"4","resultStr":"{\"title\":\"RNA-seq analysis of gene expression profiles in posttraumatic stress disorder, Parkinson's disease and schizophrenia identifies roles for common and distinct biological pathways.\",\"authors\":\"Sian M J Hemmings, Patricia Swart, Jacqueline S Womersely, Ellen S Ovenden, Leigh L van den Heuvel, Nathaniel W McGregor, Stuart Meier, Soraya Bardien, Shameemah Abrahams, Gerard Tromp, Robin Emsley, Jonathan Carr, Soraya Seedat\",\"doi\":\"10.1007/s44192-022-00009-y\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Evidence suggests that shared pathophysiological mechanisms in neuropsychiatric disorders (NPDs) may contribute to risk and resilience. We used single-gene and network-level transcriptomic approaches to investigate shared and disorder-specific processes underlying posttraumatic stress disorder (PTSD), Parkinson's disease (PD) and schizophrenia in a South African sample. RNA-seq was performed on blood obtained from cases and controls from each cohort. Gene expression and weighted gene correlation network analyses (WGCNA) were performed using DESeq2 and CEMiTool, respectively. Significant differences in gene expression were limited to the PTSD cohort. However, WGCNA implicated, amongst others, ribosomal expression, inflammation and ubiquitination as key players in the NPDs under investigation. Differential expression in ribosomal-related pathways was observed in the PTSD and PD cohorts, and focal adhesion and extracellular matrix pathways were implicated in PD and schizophrenia. We propose that, despite different phenotypic presentations, core transdiagnostic mechanisms may play important roles in the molecular aetiology of NPDs.</p>\",\"PeriodicalId\":72827,\"journal\":{\"name\":\"Discover mental health\",\"volume\":\" \",\"pages\":\"6\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2022-03-03\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10501040/pdf/\",\"citationCount\":\"4\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Discover mental health\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1007/s44192-022-00009-y\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Discover mental health","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/s44192-022-00009-y","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
RNA-seq analysis of gene expression profiles in posttraumatic stress disorder, Parkinson's disease and schizophrenia identifies roles for common and distinct biological pathways.
Evidence suggests that shared pathophysiological mechanisms in neuropsychiatric disorders (NPDs) may contribute to risk and resilience. We used single-gene and network-level transcriptomic approaches to investigate shared and disorder-specific processes underlying posttraumatic stress disorder (PTSD), Parkinson's disease (PD) and schizophrenia in a South African sample. RNA-seq was performed on blood obtained from cases and controls from each cohort. Gene expression and weighted gene correlation network analyses (WGCNA) were performed using DESeq2 and CEMiTool, respectively. Significant differences in gene expression were limited to the PTSD cohort. However, WGCNA implicated, amongst others, ribosomal expression, inflammation and ubiquitination as key players in the NPDs under investigation. Differential expression in ribosomal-related pathways was observed in the PTSD and PD cohorts, and focal adhesion and extracellular matrix pathways were implicated in PD and schizophrenia. We propose that, despite different phenotypic presentations, core transdiagnostic mechanisms may play important roles in the molecular aetiology of NPDs.